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15 Cards in this Set

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Ziemann et al (1977)

- Reduced control theory – lack of ability to suppress in sensory andlimbic areas leads to premonitory urges, reduced inhibition in the motor areas= ticsThis theory suggests that lack ofinhibitory control leads to TS syndrome, but there is a debate over whetherthis is actually the case: Mixed findings for cognitive controlin with some studies having suggested to have enhanced cognitive control in TS


CSTC loop

Cortico-striatal-thalamic-cortical loops


The BG is involved in the selection ofaction, which also involves the simultaneous suppression or inhibition ofirrelevant actions. In the striatum, GABA is the main inhibitoryneurotransmitter and the suggestion is that decreased levels of GABA in thestriatum result in an inability to supress irrelevant actions and thereforeshow reduced control.

Kalithini et al., (2005)

Post-mortemstudies have shown reduced GABA concentrations in the


Bronfield et al (2011)


Furthermore,animal models of TS have demonstrated that GABA antagonism results in theexpression of tic like behaviour


MSN’s in the striatum becomeinappropriately active, and loose specificity – whereas they are normally veryselective, see spikes in firing rates with recuced GABA. This in turn resultsin phasic inhibition of tonically active inhibitory cells therefore having anet effect of disinhibition.


Orthet al (2008)


Sothe disinhibition of the thalamus leads to a hyper-excitable cortex, andtherefore reduced cognitive control


demonstrated that patients had reduced SICI when at rest – indicates ahyper-excitable cortex.


Church et al (2009)


adolescentswith TS may have less effective functional communication between distant areasof cortex, and in contrast, ‘over’ communication between regions in closeproximity, similar to younger children – this could help explain the inabilityto suppress unwanted behaviours


Yaniv et al (2017)

Battery of EF tasks given to adults whopreviously had TS – done in adults as how can we judge EF in children whentheir EF areas have not fully developed yet. Findings suggest that the mainexecutive component impaired in adult TS patients is response inhibitionability regardless to the presence of comorbid ADHD. No evidence for increasedcontrol.


Expresses the need for longitudinal studies to see how EF changesover time.


Dursan et al (2000)

antisaccadetask on six male Tourette syndrome patients and neurotypical controls. Theantisaccade RT and the error rates were significantly higher in the Tourettesyndrome group compared to the control group.

Poor EC due to dysfunction of frontocortico-strial network

Heise et al (2010)


REDUCED GAIN OF TMS-INDUCED MOTOREXCITABILITY AND GAIN OF MOTOR EXCITABILITY IMMEDIATELY PRIOR TO VOLITIONALMOVEMENTS SEEN IN TS PATIENTS. In controls can see that as the response isabout to be made, motor excitability goes up, however in TS this motorexcitability is reduced - it is actively being suppressed. TS patients showedsignificant disinhibition at rest. During movement preparation, see a suddenincrease in inhibition.è While inhibition during the resting state is far below the level ofcontrol subjects, and the cortical excitability is higher, task-relatedmodulation of cortical excitability reveals the capacity to inhibit effectivelyan inappropriate rise of excitability.


Jackson et al (2011)

oculomotor switchingtask. On repeat trials there is no difference between people with TS andcontrols. On switch trials can actually see that people with TS do better. Theyshow increased cognitive control and are much more accurate, and just as quick.


- People with TS spend large amounts of timetrying to suppress tics and this enhances cognitive control mechanisms – thisenhanced cog control spills very onto the task.


- TS patients with normal switch costs show worsetics.


Worbe et al (2015)

Specifically, striatum and thalamus hadabnormally enhanced structural connectivity with primary motor and sensorycortices and this enhanced connectivity positively correlated with tic severityFrontalareas also had enhanced connectivity with the striatum, and this was independent of tics. Taking into account that thesecortical areas are involved in behavioural stopping and switching and thatpatients with TS often display an enhanced cognitive control over theirmovements, structural changes could also reflect plastic brain reorganizationin GTS.è some of these structuralchanges could be related to the presence of co-morbidities. Indeed, theseverity of OCD in adult patients with GTS was positively correlated tostructural connections of the striatum and thalamus with the medialorbito-frontal cortexBUT – increased connectivity associated with noisy signals and worsetics, so perhaps it isn’t adaptive but a cause.


Contradictory evidence for connectivitydifferences




Cavanna et al (2010)


BUT


Tinaz et al (2015)

Cavannaet al (2010

AssessedCC in MZ twins, discordant for TS. No difference structurally but TS one hadlow connectivity in the CC – this reduced connectivity can be seen as anadaptation to the disorder to create less noisy signals.

Tinazet al (2015)

Increasedconnectedness of the right dorsal anterior insula with the thalamus and putamencorrelated with worsened clinical symptoms. BUTputting twitchy people in fMRI scanners and telling them not to move.


Conclusion;


Very mixed evidencebut it appears, overall TS patients are not impaired in cognitive control ofvoluntary movements, but are impaired in the suppression of tics. SO, whilstthey do seem to display evidence of impaired cog control, compensatoryadaptations in brain structure and function mean that in some respects theyhave enhanced cognitive control – or at least those that learn to control theirtics do.è Either way, it is clear that cognitive control is abnormal and verycomplexè Mixed resuts likely due to heterogeneity of the tasks and ofpatients used.